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Finally some researchers are starting to poke in the right direction, at least relative to my theory. Of course they are interpreting it in terms of immune system modulation. Just a shame they don't look at it from my view: as spermine synthase over-expression in the targeted brain cells following inactive X chromosome fragmentation. Spermine synthase is on the 2 X chromosomes in female cells but usually only one copy is expressed, from the active X.

Also, they are picking on those poor EAE rats again.

The first article is really old and all I can post is the title. The second article (abstract) is more recent.

The polyamine biosynthetic pathway is a therapeutic target for proliferative diseases because cellular proliferation requires elevated levels of polyamines. A byproduct of the latter stages of polyamine biosynthesis (the synthesis of spermidine and spermine) is 5'-methylthioadenosine (MTA).

In humans, MTA is processed by 5'-methylthioadenosine phosphorylase (MTAP) so that significant amounts of MTA do not accumulate. Potent inhibitors of MTAP might allow the buildup of sufficient levels of MTA to generate feedback inhibition of polyamine biosynthesis.

We have designed and synthesized a family of potential transition-state analogue inhibitors of MTAP on the basis of our knowledge of the transition-state structure of purine nucleoside phosphorylase and the assumption that it is likely the two enzymes share a common catalytic mechanism. Several of the inhibitors display slow-onset tight-binding properties, consistent with them being transition-state analogues, with the most potent having a dissociation constant of 166 pM.

MTA is actually created as a product of polyamine (spermine and spermidine) synthesis. So it is in each cell in low amounts. It is quickly converted to phospho-MTA and then back to methionine to create more S-adenosylmethionine (SAM).
SAM is important for methylation of DNA and histone (and other proteins) to help in gene silencing and packaging. In competition with this use of SAM, SAM is decarboxylated by SAM decarboxylase creating dcSAM for use in polyamine synthesis. For spermidine synthesis by the enzyme spermidine synthase, dcSAM and putrescine are converted to spermidine and MTA. For spermine synthesis by the enzyme spermine synthase, dcSAM and spermidine are converted to spermine and MTA.
So, by providing an abundance of the product MTA, it backs up the polyamine synthesis. Increases in polyamines are necessary in cell proliferation, such as in T-cell expansion in reaction to an antigen.
If you are converted spermidine to spermine faster than you can replenish the spermidine due to extra expression of spermine synthase (as I am suggesting), then you are reducing the cell's spermidine. Spermidine is essential in a cell for a very unique control (I believe it is translation control). Spermidine is ligated to an elongation factor and converted to a rare amino acid hypusine. Without this, the cell will not live. Also, increased spermine (+4) could cause more stabilization of alternate protein and DNA complexes (such as Z-DNA), compared to spermidine (+3). Normal there is a balance in the spermine/spermidine ratio. I have referred previously to the Quaking and Jimpy mouse strains that have progressive neurodegeneration. They were shown to have changes in their spermine/spermidine ratios and amounts relative to control mice.
I don't know if you can buy MTA as a drug. I am in drug discovery and have a potential drug candidate for SAM decarboxylase for cancer therapy. I am hoping to work on spermine synthase for drug discovery but it would be for cancer treatment. As it is, I have about 15 other cancer related targets I am working on, so not much time to work on what interests me most.

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